2026-06-23 | Auer Rod-Like Inclusions in T-cell Large Granular Lymphocytic Leukaemia.
A 71-year-old man presented with cytopenias and splenomegaly. Diagnostic workup revealed T-cell large granular lymphocytic leukemia (T-LGLL), characterized by a clonal CD8+ T-cell population with STAT3 mutation. A rare morphological finding of myeloperoxidase-negative Auer rod-like inclusions in the leukemic lymphocytes was observed, a feature seldom reported in this T-cell malignancy.
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2026-06-17 | Observation of Hematologic Improvement with Luspatercept in Patients with Anemia from Diverse Hematologic Disorders: A Single-Center Retrospective Clinical Analysis
Background: Anemia is a common clinical condition in hematology, associated with diverse etiologies and treatment strategies, many of which have notable limitations. Luspatercept, a novel erythroid maturation agent, has shown promise in treating anemia, particularly in patients with β-thalassemia and myelodysplastic syndromes (MDS). This study aimed to evaluate the real-world hematologic effectiveness of luspatercept across various anemia subtypes. Materials and Methods: A retrospective observational study was conducted on 22 patients with anemia of different origins—MDS, post-hematopoietic stem cell transplantation (HSCT), aplastic anemia (AA), and T-cell large granular lymphocytic leukemia (T-LGLL)—who received luspatercept therapy at the 960th Hospital from June 2023 to January 2025. Hematologic improvement was assessed using the International Working Group (IWG) 2018 criteria for erythroid response (HI-E). Pre- and post-treatment changes in hemoglobin (Hb), reticulocyte percentage (RET %), and absolute reticulocyte count (RET #) were analyzed using the Wilcoxon Signed-Rank Test. Multivariate regression was employed to control for age, gender, and disease severity. Statistical significance was set at P ≤ 0.05, and all analyses were performed using SPSS version 27.0. Results: Among the 22 patients, 10 (45.5%) had MDS (5 low-risk, 5 intermediate-to-high-risk), 6 (27.3%) post-HSCT anemia, 4 (18.2%) AA, and 2 (9%) T-LGLL. A total of 16 patients (72.7%) achieved a clinically meaningful erythroid response. Seven (43.8%) of these remained transfusion-independent until the last follow-up, with a median duration of 19.5 weeks (range: 8.6–47). Median time to initial response was 3.86 weeks (range: 0.57–25.57). Significant increases were observed in Hb (P < 0.001) and RET # (P = 0.001), while the increase in RET % did not reach statistical significance (P = 0.088). These findings support the efficacy of luspatercept in promoting erythropoiesis and improving anemia in a heterogeneous patient population. Conclusion: Luspatercept demonstrated significant hematologic improvement, particularly in hemoglobin levels, in patients with anemia from various hematologic disorders. These results support its broader therapeutic potential. Future multicenter, prospective studies are warranted to validate its role in treating other forms of anemia.
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2026-06-06 | T-cell large granular lymphocyte leukaemia with pure red cell aplasia harbouring a somatic STAT3 P715L mutation.
T-cell large granular lymphocyte leukaemia (T-LGLL) is a chronic lymphoproliferative disorder often associated with pure red cell aplasia (PRCA). We report a unique case of a woman in her 50s presenting with PRCA secondary to T-LGLL, in which targeted next-generation sequencing identified a somatic STAT3 P715L mutation. This variant, previously described only in germline mutation in STAT3 gain-of-function syndrome, has not been reported as a somatic mutation in T-LGLL. Immunohistochemical analysis revealed constitutive STAT3 (signal transducer and activator of transcription 3) activation in clonal CD8+ T cells, suggesting a pathogenic role for the P715L mutation. The patient responded to ciclosporin therapy with gradual haematological improvement and became transfusion-independent within 6 months. This case highlights the importance of molecular profiling in T-LGLL presentations and expands the known mutational spectrum of STAT3 It also raises the possibility that non-SH2 (Src homology 2) domain STAT3 mutations may contribute to disease pathogenesis and influence treatment response in T-LGLL.
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